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Summary Background Infection is the most common cause of mortality in end-stage liver disease (ESLD). The impact of obesity on infection risk in ESLD is not established. Aim To characterise the impact of obesity on infection risk in ESLD. Methods We evaluated the association between infection and obesity in patients with ESLD. Patients grouped as non-obese, obesity class I–II and obesity class III were studied using the Nationwide Inpatient Sample. Validated diagnostic code based algorithms were utilised to determine weight category and infections, including bacteraemia, skin/soft tissue infection, urinary tract infection (UTI), pneumonia/respiratory infection, Clostridium difficile infection (CDI) and spontaneous bacterial peritonitis (SBP). Risk factors for infection and mortality were assessed using multivariable logistic regression analysis. Results Of 115 465 patients identified, 100 957 (87.5%) were non-obese and 14 508 (12.5%) were obese, with 9489 (8.2%) as obesity class I–II and 5019 (4.3%) as obesity class III. 37 117 patients (32.1%) had an infection diagnosis. Infection was most prevalent among obesity class III (44.0%), followed by obesity class I–II (38.9%) and then non-obese (31.9%). In multivariable modelling, class III obesity (OR = 1.41; 95% CI 1.32–1.51; P < 0.001), and class I–II obesity (OR = 1.08; 95% CI 1.01–1.15; P = 0.026) were associated with infection. Compared to non-obese patients, obese individuals had greater prevalence of bacteraemia, UTI, and skin/soft tissue infection as compared to non-obese patients. Conclusions Obesity is newly identified to be independently associated with infection in end-stage liver disease. The distribution of infection sites varies based on weight category.

Background/Aims: Noting the contribution to renal transplantation by the introduction of the laparoscopic approach to donor nephrectomy, we investigated the possibility of performing a laparoscopic hepatic lobe procurement with the goal of performing a live donor liver transplantation. We describe our technique and determine its feasibility for such a goal. Methods: The surgical technique was developed over a series of 12 adult female pigs and adapted in two human cadavers. The technique included pneumoperitoneum with CO 2 , mobilization of the liver, and transection of the parenchyma into right and left lobes with a laparoscopic cavitron ultrasonic aspirator. The vascular inflow and outflow structures (hepatic artery, portal vein, hepatic veins) of the anatomical specimen being procured were preserved undisturbed during the hepatic transection. No temporary vascular occlusion techniques were utilized. The vascular structures were stapled and sectioned just prior to removal of the specimen. Results: Hepatic lobectomies were successfully performed laparoscopically. Vascular and biliary structures were preserved to allow for subsequent transplantation. Operative time from establishment of pneumoperitoneum to lobe procurement was under 4 h. Conclusions: This study demonstrates the feasibility of laparoscopic living donor procurement for liver transplantation, from both a technical and a physiological perspective.

Liver transplantation is the option for end-stage liver diseases. Shortage of donor liver organ is a major issue. To overcome this, alternative approaches including hepatic cell transplantation, bioartificial liver devise and whole liver organ engineering are being investigated. We focus on developing engineered liver using natural liver scaffold generated via decellularization process. The liver scaffold would maintain the authentic three- dimensional micro-architecture and vasculature. The liver scaffold repopulated with patient-specific hepatic cells differentiated from induced pluripotent stem cells (iPSC) is a promising option. For this proof-of-concept study, we decellularized rat liver by perfusing detergents SDS and Triton x-100. Histological analysis of decellularized liver matrix (DLM) revealed removal of cellular component and preservation of extra-cellular architecture. Presence of collagen type IV and laminin in the DLM was verified. Human endothelial cells seeded through DLM portal vein pres...

Tacrolimus is an effective immunosuppressant in the rescue of liver allograft patients in whom conventional immunosuppression failed. Efficacy and safety were examined in a multicenter trial of liver transplant recipients converted to tacrolimus because of rejection despite cyclosporine (CyA) therapy or intolerance to CyA. Six hundred seventy-seven patients were enrolled onto the study; 475 patients for rejection, 197 patients for intolerance, and 5 patients treated compassionately. The mean daily dose of tacrolimus was less in the intolerance (Int) patients throughout the study: 0.22 versus 0.17 mg/kg at 1 week and 0.14 versus 0.11 mg/kg at 24 months in rejection (Rej) and Int patients, respectively. Mean blood levels paralleled dosing in both groups, but were greater in the Rej patients (10.7 v 8.3 ng/mL at 18 months). Kaplan-Meier estimates of patient and graft survival were similar in the two groups. Patient survival rates were 80.1% and 81.5%, and graft survival rates were 72.7% and 73.9% at 24 months in the Rej and Int patients, respectively. Most adverse events occurred with a similar incidence in the two groups. Those with a 4% or greater incidence were fever, viral hepatitis, and pneumonia. The incidence of sepsis, gastrointestinal hemorrhage, kidney failure, and convulsion was greater in the Int group. The incidence of abnormal liver function test results, hyperglycemia, headache, and abnormal kidney function was greater in the Rej group. Mean liver function test results decreased with time postrescue in both groups. Mean serum creatinine level increased from baseline to 18 months postrescue in both groups (1.44 to 1.51 mg/dL for Int patients, 1.14 to 1.48 mg/dL for Rej patients). We conclude tacrolimus is safe and effective rescue in liver transplant recipients with rejection or CyA intolerance.

Obesity is associated with an increased incidence of infection, diabetes, and cardiovascular disease, which together account for most obesity-related morbidity and mortality. Decreased expression of leptin or of functional leptin receptors results in hyperphagia, decreased energy expenditure, and obesity. It is unclear, however, whether defective leptin-dependent signal transduction directly promotes any of the conditions that frequently complicate obesity. Abnormalities in tumor necrosis factor α expression have been noted in each of the above comorbid conditions, so leptin deficiency could promote these complications if leptin had immunoregulatory activity. Studies of rodents with genetic abnormalities in leptin or leptin receptors revealed obesity-related deficits in macrophage phagocytosis and the expression of proinflammatory cytokines both in vivo and in vitro. Exogenous leptin up-regulated both phagocytosis and the production of proinflammatory cytokines. These results identify an important and nov...

The vascular supply of the liver and gallbladder is characterized by a striking degree of polymorphism. The occurrence of variants that differ from the usual pattern is both surprisingly common and unpredictable. Knowledge of this variable anatomy is particularly important during surgical interventions in which preoperative imaging studies are not available, such as in organ procurements. In this report we consider various anatomical arterial configurations, and describe an unusual variant.